Background: Noise-induced hearing loss (NIHL) is a kind of acquired sensorineural hearing loss and has shown an increasing incidence in recent years. Hence, elucidating the exact pathophysiological mechanisms and proposing effective treatment and prevention methods become the top priority. Though a great number of researches have been carried out on NIHL, few of them were focused on metabolites.
Aims/objectives: To reveal the metabolomic changes in cochlear fluid after noise injury and search for underlying inner ear biomarkers of NIHL.
Material and methods: In this study, cochlea fluid extracted from guinea pigs after impulse noise exposure were subjected to GC-MS and LC-MS untargeted metabolomics analysis.
Results: After impulse noise exposure, 62 significantly changed metabolites in guinea pig cochlea fluid were screened out and deoxyribose 1-phosphate was selected as the key metabolite and underlying biomarker for NIHL. KEGG pathway analysis showed that oxidative phosphorylation, glycerophospholipid metabolism, pyrimidine metabolism and pentose phosphate pathway were significantly changed at all observed time points after noise.
Conclusions and significance: This study effectively promoted the application of metabolomics in hearing research. The pathophysiology process of NIHL in the inner ear was closely connected with oxidative phosphorylation, glycerophospholipid metabolism, pyrimidine metabolism and pentose phosphate pathway and deoxyribose 1-phosphate could be the biomarker for NIHL.
Keywords: Noise-induced hearing loss; biomarker; cochlear fluid; deoxyribose 1-phosphate; metabolomics.